Institution
Ochsner Medical Center
Healthcare•New Orleans, Louisiana, United States•
About: Ochsner Medical Center is a healthcare organization based out in New Orleans, Louisiana, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 980 authors who have published 1159 publications receiving 49961 citations. The organization is also known as: Ochsner Hospital & Ochsner Foundation Hospital.
Papers published on a yearly basis
Papers
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TL;DR: It is believed that the authors are now in a very exciting era in which a multifactorial approach to the primary and secondary prevention of coronary artery disease is needed in order to further reduce morbidity and mortality rates.
Abstract: We review data from our institution demonstrating the benefits of cardiac rehabilitation and exercise training on coronary risk factors, exercise capacity, behavioral characteristics, and quality of life in various subgroups of patients. In addition, we discuss our research in several other areas of preventive cardiology, including lipid disorders, hypertension, left ventricular hypertrophy, fish oils, and antioxidants. We believe that we are now in a very exciting era in which a multifactorial approach to the primary and secondary prevention of coronary artery disease is needed in order to further reduce morbidity and mortality rates.
14 citations
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TL;DR: The authors showed that differences in the type, function and transcriptome of Granulocytic-MDSC may explain the severity of COVID-19, in particular the association with pulmonary complications.
Abstract: COVID-19 ranges from asymptomatic in 35% of cases to severe in 20% of patients. Differences in the type and degree of inflammation appear to determine the severity of the disease. Recent reports show an increase in circulating monocytic-myeloid-derived suppressor cells (M-MDSC) in severe COVID 19, that deplete arginine but are not associated with respiratory complications. Our data shows that differences in the type, function and transcriptome of Granulocytic-MDSC (G-MDSC) may in part explain the severity COVID-19, in particular the association with pulmonary complications. Large infiltrates by Arginase 1 + G-MDSC (Arg + G-MDSC), expressing NOX-1 and NOX-2 (important for production of reactive oxygen species) were found in the lungs of patients who died from COVID-19 complications. Increased circulating Arg + G-MDSC depleted arginine, which impaired T cell receptor and endothelial cell function. Transcriptomic signatures of G-MDSC from patients with different stages of COVID-19, revealed that asymptomatic patients had increased expression of pathways and genes associated with type I interferon (IFN), while patients with severe COVID-19 had increased expression of genes associated with arginase production, and granulocyte degranulation and function. These results suggest that asymptomatic patients develop a protective type I IFN response, while patients with severe COVID-19 have an increased inflammatory response that depletes arginine, impairs T cell and endothelial cell function, and causes extensive pulmonary damage. Therefore, inhibition of arginase-1 and/or replenishment of arginine may be important in preventing/treating severe COVID-19.
14 citations
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TL;DR: A case of Wilms' tumor is reported in a 13-month-old boy who, after radical left nephrectomy, developed a left testicular mass that turned out to be metastatic Wilm's tumor.
Abstract: Wilms' tumors account for the vast majority of renal neoplasms in infants and children. Common areas for metastases include the lung, liver, and contralateral kidney. Less common sites include the bone, skin, brain, and orbit. We report a case of Wilms' tumor in a 13-month-old boy who, after radical left nephrectomy, developed a left testicular mass that turned out to be metastatic Wilms' tumor. The epidemiology, case history, review of the literature, and possible etiology of this rare site of metastatic Wilms' tumor are discussed.
14 citations
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TL;DR: Although obesity causes anomalies in diastolic and systolic functioning and although it might be expected to increase the risk of mortality in patients with established heart failure, the group and others have shown that, paradoxically, BMI is inversely related to mortality over the long term in Patients with chronic heart failure.
Abstract: Obesity is a well-known independent risk factor for heart failure 1 and has now reached epidemic proportions: the World Health Organization calculates that there are over 1000 million overweight adults worldwide and that 300 million of them are clinically obese. The incidence and prevalence of obesity and heart failure are so high that it is not unusual to find both conditions in the same patient. In fact, several cohort studies of heart failure patients have shown that 15%-35% of those patients are obese and that 30%-60% are overweight. 2 Epidemiological studies have clearly shown a close relationship between obesity and an increased risk of cardiovascular disease (CVD) and mortality in the general population. However, in some of those studies a U- or J-curve was observed, indicating that mortality is higher in individuals with a low body mass index (BMI). 2-4 Uncovering the relationship between obesity and heart failure is turning out to be complex. A recent epidemiological study derived from the Framingham Heart Study clearly showed that obesity and overweight are highly predictive of later clinical heart failure. Although obesity causes anomalies in diastolic and systolic functioning and although it might be expected to increase the risk of mortality in patients with established heart failure, our group and others have shown that, paradoxically, BMI is inversely related to mortality over the long term in patients with chronic heart failure. 2,3,5-11 BMI is not the only conventional risk factor to present a paradoxical association with clinical outcomes in heart failure patients. High concentrations of low density lipoproteins and total cholesterol have also been associated with a survival advantage in heart failure patients. These systematic findings for different risk factors in heart failure patients justify the use of the term “reverse epidemiology.” 10
14 citations
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TL;DR: The treatment outcomes in adult patients with type 2 diabetes enrolled in the GetGoal trials of lixisenatide (LIXI) and the predictive effects of baseline characteristics on outcomes are explored.
Abstract: Aims
To explore the treatment outcomes in adult patients with type 2 diabetes (T2D) enrolled in the GetGoal trials of lixisenatide (LIXI), and the predictive effects of baseline characteristics on outcomes.
Methods
This study was a pooled analysis of patient-level data from LIXI GetGoal studies comparing LIXI and placebo. Patients were divided into baseline therapy groups: oral antihyperglycaemic drugs (OADs) at baseline (n = 2,760) or basal insulin at baseline (n = 1,198).
Results
LIXI treatment, compared to placebo, led to significantly greater reduction in glycated haemoglobin (HbA1c), and greater achievement of the composite endpoint of HbA1c <7.0% (53 mmol/mol) with no symptomatic hypoglycaemia and no weight gain in both the OAD (34% vs 18%, p < 0.0001) and basal insulin groups (19% vs 10%, p < 0.0001). Treatment with LIXI was associated with a greater percentage of patients experiencing a symptomatic hypoglycaemic event compared with placebo in both the OAD (5% vs 3%, p = 0.0098) and basal insulin (27% vs 17%, p < 0.0001) groups. In assessing baseline factors that were predictors of treatment outcomes, only baseline HbA1c and LIXI treatment were strong predictors of outcomes in both the OAD and basal insulin groups. No other baseline characteristic had as large or as consistent clinically relevant predictive effect across treatment outcomes.
Conclusions
The results from this study show that irrespective of baseline characteristics, LIXI treatment, as an add-on to OAD or basal insulin therapy, is effective in reducing HbA1c and achieving composite endpoints.
14 citations
Authors
Showing all 993 results
Name | H-index | Papers | Citations |
---|---|---|---|
Carl J. Lavie | 106 | 1135 | 49318 |
Michael R. Jaff | 82 | 442 | 28891 |
Michael F. O'Rourke | 81 | 451 | 35355 |
Mandeep R. Mehra | 80 | 644 | 31939 |
Richard V. Milani | 80 | 454 | 23410 |
Christopher J. White | 77 | 621 | 25767 |
Bruce A. Reitz | 74 | 333 | 18457 |
Robert C. Bourge | 69 | 273 | 24397 |
Sana M. Al-Khatib | 69 | 377 | 17370 |
Hector O. Ventura | 66 | 478 | 16379 |
Andrew Mason | 63 | 360 | 15198 |
Aaron S. Dumont | 60 | 386 | 13020 |
Philip J. Kadowitz | 55 | 379 | 11951 |
David W. Dunn | 54 | 195 | 8999 |
Lydia A. Bazzano | 51 | 267 | 13581 |